ReviewInternational journal of hematology2010
Molecular aspects of myeloproliferative neoplasms.
Review in International journal of hematology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 73 citations in OpenAlex.
- SIMPLIFY-1: A Phase III Randomized Trial of Momelotinib Versus Ruxolitinib in Janus Kinase Inhibitor-Naïve Patients With Myelofibrosis.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2017Trial
- A double-blind, placebo-controlled trial of ruxolitinib for myelofibrosis.The New England journal of medicine · 2012Trial
- The molecular management of classic myeloproliferative neoplasm.Journal of the Egyptian National Cancer Institute · 2025Review
- Lysyl oxidase like-2 in fibrosis and cardiovascular disease.American journal of physiology. Cell physiology · 2023Review
- Allelic burden of Janus kinase 2 in a 6-month course of therapy for myeloproliferative neoplasms.Molecular biology reports · 2023Article
- Putative Role of Neutrophil Extracellular Trap Formation in Chronic Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Review
- Reduced-intensity conditioning versus myeloablative conditioning allogeneic stem cell transplantation for patients with myelofibrosis.Blood research · 2022Article
- Circulating Endothelial Cell Levels Correlate with Treatment Outcomes of Splanchnic Vein Thrombosis in Patients with Chronic Myeloproliferative Neoplasms.Journal of personalized medicine · 2022Article
- Neutrophil Death in Myeloproliferative Neoplasms: Shedding More Light on Neutrophils as a Pathogenic Link to Chronic Inflammation.International journal of molecular sciences · 2022Review
- Low-dose ruxolitinib shows effective in treating myelofibrosis.Annals of hematology · 2021Article
- A Phase I, Randomized, Double-Blind, Placebo-Controlled, Single Ascending Dose, Multiple Ascending Dose and Food Effect Study to Evaluate the Tolerance, Pharmacokinetics of Jaktinib, a New Selective Janus Kinase Inhibitor in Healthy Chinese Volunteers.Frontiers in pharmacology · 2020Article
- The Role of Caspase Genes Polymorphisms in Genetic Susceptibility to Philadelphia-Negative Myeloproliferative Neoplasms in a Portuguese Population.Pathology oncology research : POR · 2019Article
- Efficacy of ruxolitinib retreatment in a patient with high-risk myelofibrosis using the international prognostic scoring system.Drugs in context · 2019Article
- Ruxolitinib therapy for myelofibrosis in Austria : Consensus on therapy management.Wiener klinische Wochenschrift · 2018Article
- β-Arrestin2 mediates progression of murine primary myelofibrosis.JCI insight · 2017Article
- Prevalence of the Janus kinase 2 V617F mutation in Philadelphia-negative myeloproliferative neoplasms in a Portuguese population.Biomedical reports · 2017Article
- DNA repair genes polymorphisms and genetic susceptibility to Philadelphia-negative myeloproliferative neoplasms in a Portuguese population: The role of base excision repair genes polymorphisms.Oncology letters · 2017Article
- Coexistence of JAK2 and CALR mutations and their clinical implications in patients with essential thrombocythemia.Oncotarget · 2016Article
- JAK-STAT pathway activation in malignant and nonmalignant cells contributes to MPN pathogenesis and therapeutic response.Cancer discovery · 2015Article
- Identification of AIM2 as a downstream target of JAK2V617F.Experimental hematology & oncology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During these past 5 years several studies have provided major genetic insights into the pathogenesis of the so-called classical myeloproliferative neoplasms (MPNs): polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The discovery of the JAK2V617F mutation first, then of the JAK2 exon 12 and MPLW515 mutations, have modified the understanding of these diseases, their diagnosis, and management. Now it is established that almost 100% of PV patients present a JAK2 mutation. Nearly 60% of ET patients and 50% of patients with PMF have the JAK2V617F mutation. The MPLW515 mutations are also present in a small proportion of ET and PMF patients. These mutations are oncogenic events that cause these disorders; however, they do not explain the heterogeneity of the entities in which they occur. Genetic defects have not been yet identified in around 40% of ET and PMF. There are likely additional somatic genetic factors important for the MPN phenotype like the recently described TET2, ASXL1, and CBL mutations. Moreover, polymorphisms in the JAK2 gene have been recently described as associated with MPN. Additional studies of large cohorts are required to dissect the genetic events in MPNs and the mechanisms of these oncogenic cooperations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.